An ABO blood grouping discrepancy: Probable B(A) phenotype
In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, A...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Jain, Ashish [verfasserIn] |
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| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
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| Umfang: |
2 |
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| Übergeordnetes Werk: |
Enthalten in: Pro-Resolving Lipid Mediators Modulate the NLRP3 Inflammasome in Chronic Liver Disease - Lopategi, A. ELSEVIER, 2016, official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis, Oxford |
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| Übergeordnetes Werk: |
volume:56 ; year:2017 ; number:3 ; pages:459-460 ; extent:2 |
| Links: |
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| DOI / URN: |
10.1016/j.transci.2017.05.002 |
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ELV030294762 |
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| 520 | |a In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. | ||
| 520 | |a In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. | ||
| 700 | 1 | |a Gupta, Anubhav |4 oth | |
| 700 | 1 | |a Malhotra, Sheetal |4 oth | |
| 700 | 1 | |a Marwaha, Neelam |4 oth | |
| 700 | 1 | |a Sharma, Ratti Ram |4 oth | |
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10.1016/j.transci.2017.05.002 doi GBVA2017004000026.pica (DE-627)ELV030294762 (ELSEVIER)S1473-0502(17)30084-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.44 bkl Jain, Ashish verfasserin aut An ABO blood grouping discrepancy: Probable B(A) phenotype 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. Gupta, Anubhav oth Malhotra, Sheetal oth Marwaha, Neelam oth Sharma, Ratti Ram oth Enthalten in Elsevier [u.a.] Lopategi, A. ELSEVIER Pro-Resolving Lipid Mediators Modulate the NLRP3 Inflammasome in Chronic Liver Disease 2016 official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis Oxford (DE-627)ELV01380703X volume:56 year:2017 number:3 pages:459-460 extent:2 https://doi.org/10.1016/j.transci.2017.05.002 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_26 GBV_ILN_40 GBV_ILN_252 44.44 Parasitologie Medizin VZ AR 56 2017 3 459-460 2 045F 610 |
| spelling |
10.1016/j.transci.2017.05.002 doi GBVA2017004000026.pica (DE-627)ELV030294762 (ELSEVIER)S1473-0502(17)30084-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.44 bkl Jain, Ashish verfasserin aut An ABO blood grouping discrepancy: Probable B(A) phenotype 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. Gupta, Anubhav oth Malhotra, Sheetal oth Marwaha, Neelam oth Sharma, Ratti Ram oth Enthalten in Elsevier [u.a.] Lopategi, A. ELSEVIER Pro-Resolving Lipid Mediators Modulate the NLRP3 Inflammasome in Chronic Liver Disease 2016 official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis Oxford (DE-627)ELV01380703X volume:56 year:2017 number:3 pages:459-460 extent:2 https://doi.org/10.1016/j.transci.2017.05.002 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_26 GBV_ILN_40 GBV_ILN_252 44.44 Parasitologie Medizin VZ AR 56 2017 3 459-460 2 045F 610 |
| allfields_unstemmed |
10.1016/j.transci.2017.05.002 doi GBVA2017004000026.pica (DE-627)ELV030294762 (ELSEVIER)S1473-0502(17)30084-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.44 bkl Jain, Ashish verfasserin aut An ABO blood grouping discrepancy: Probable B(A) phenotype 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. Gupta, Anubhav oth Malhotra, Sheetal oth Marwaha, Neelam oth Sharma, Ratti Ram oth Enthalten in Elsevier [u.a.] Lopategi, A. ELSEVIER Pro-Resolving Lipid Mediators Modulate the NLRP3 Inflammasome in Chronic Liver Disease 2016 official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis Oxford (DE-627)ELV01380703X volume:56 year:2017 number:3 pages:459-460 extent:2 https://doi.org/10.1016/j.transci.2017.05.002 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_26 GBV_ILN_40 GBV_ILN_252 44.44 Parasitologie Medizin VZ AR 56 2017 3 459-460 2 045F 610 |
| allfieldsGer |
10.1016/j.transci.2017.05.002 doi GBVA2017004000026.pica (DE-627)ELV030294762 (ELSEVIER)S1473-0502(17)30084-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.44 bkl Jain, Ashish verfasserin aut An ABO blood grouping discrepancy: Probable B(A) phenotype 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. Gupta, Anubhav oth Malhotra, Sheetal oth Marwaha, Neelam oth Sharma, Ratti Ram oth Enthalten in Elsevier [u.a.] Lopategi, A. ELSEVIER Pro-Resolving Lipid Mediators Modulate the NLRP3 Inflammasome in Chronic Liver Disease 2016 official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis Oxford (DE-627)ELV01380703X volume:56 year:2017 number:3 pages:459-460 extent:2 https://doi.org/10.1016/j.transci.2017.05.002 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_26 GBV_ILN_40 GBV_ILN_252 44.44 Parasitologie Medizin VZ AR 56 2017 3 459-460 2 045F 610 |
| allfieldsSound |
10.1016/j.transci.2017.05.002 doi GBVA2017004000026.pica (DE-627)ELV030294762 (ELSEVIER)S1473-0502(17)30084-8 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 610 VZ 44.44 bkl Jain, Ashish verfasserin aut An ABO blood grouping discrepancy: Probable B(A) phenotype 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. Gupta, Anubhav oth Malhotra, Sheetal oth Marwaha, Neelam oth Sharma, Ratti Ram oth Enthalten in Elsevier [u.a.] Lopategi, A. ELSEVIER Pro-Resolving Lipid Mediators Modulate the NLRP3 Inflammasome in Chronic Liver Disease 2016 official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis Oxford (DE-627)ELV01380703X volume:56 year:2017 number:3 pages:459-460 extent:2 https://doi.org/10.1016/j.transci.2017.05.002 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_26 GBV_ILN_40 GBV_ILN_252 44.44 Parasitologie Medizin VZ AR 56 2017 3 459-460 2 045F 610 |
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An ABO blood grouping discrepancy: Probable B(A) phenotype |
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In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. |
| abstractGer |
In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. |
| abstract_unstemmed |
In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on group B RBCs. We herein report a case of a probable B(A) phenotype in a first time 20-year old male donor. The cell and serum grouping were done using tube technique and also with blood grouping gel card (Diaclone, ABD cards for donors, BioRad, Switzerland). The antisera used were commercial monoclonal IgM type. To check for the weak subgroup of A, cold adsorption and heat elution was performed. The cell grouping was AweakB RhD positive while the serum grouping was B. There was no agglutination with O cells and the autologous control was also negative. It was a group II ABO discrepancy with or without group IV discrepancy. Results for both the eluate and last wash were negative. Hence, the possibility of weak subgroup of A was unlikely. Blood grouping gel card also showed a negative reaction in the anti-A column. One lot of anti-A was showing ‘weak +’ agglutination while the other lot was showing ‘negative’ reaction with the donor RBCs by tube technique. There was no agglutination observed with anti-A1 lectin. Our case highlights the serological characteristics of a B(A) phenotype. This case emphasizes the vital role of cell and serum grouping in detecting such discrepancies especially in donors which can lead to mislabeling of the blood unit and may be a potential risk for the transfusion recipient if not resolved appropriately. |
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An ABO blood grouping discrepancy: Probable B(A) phenotype |
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